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http://dx.doi.org/10.1023/a:1026435103940 | DOI Listing |
J Cancer Res Clin Oncol
January 2025
Department of Pathology, Theodor Bilharz Research Institute, Giza, 12411, Egypt.
Introduction: Pancreatic ductal adenocarcinoma (PDAC) is associated with poor prognosis. The roles of the transcription factor special AT-rich binding protein-2 (SATB2) and β-catenin in PDAC have been a subject of controversy. We aimed to assess the diagnostic and prognostic impact of SATB2 and β-catenin in PDAC.
View Article and Find Full Text PDFMol Genet Genomic Med
February 2025
Department of Chemistry and Molecular Biology, Gothenburg University, Gothenburg, Sweden.
Background: SYNGAP1 encodes a Ras/Rap GTPase-activating protein that is predominantly expressed in the brain with the functional roles in regulating synaptic plasticity, spine morphogenesis, and cognition function. Pathogenic variants in SYNGAP1 have been associated with a spectrum of neurodevelopmental disorders characterized by developmental delays, intellectual disabilities, epilepsy, hypotonia, and the features of autism spectrum disorder. The aim of this study was to identify a novel SYNGAP1 gene variant linked to neurodevelopmental disorders and to evaluate the pathogenicity of the detected variant.
View Article and Find Full Text PDFFront Immunol
January 2025
Neuroimmunology Research Group, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.
Introduction: Remyelination of demyelinated axons can occur as an endogenous repair mechanism in multiple sclerosis (MS), but its efficacy varies between both MS individuals and lesions. The molecular and cellular mechanisms that drive remyelination remain poorly understood. Here, we studied the relation between microglia activation and remyelination activity in MS.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, USA.
Introduction: Iron-mediated cell death (ferroptosis) is a proposed mechanism of Alzheimer's disease (AD) pathology. While iron is essential for basic biological functions, its reactivity generates oxidants which contribute to cell damage and death.
Methods: To further resolve mechanisms of iron-mediated toxicity in AD, we analyzed post mortem human brain and ApoEFAD mice.
Alzheimers Dement
January 2025
Department of Radiology, China-Japan Friendship Hospital, Beijing, China.
Introduction: The link between overload brain iron and transcriptional/cellular signatures in Alzheimer's disease (AD) remains inconclusive.
Methods: Iron deposition in 41 cortical and subcortical regions of 30 AD patients and 26 healthy controls (HCs) was measured using quantitative susceptibility mapping (QSM). The expression of 15,633 genes was estimated in the same regions using transcriptomic data from the Allen Human Brain Atlas (AHBA).
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